Subchondral treatment of joint pain of the spine

ABSTRACT

Methods for altering the natural history of degenerative disc disease and osteoarthritis of the spine are proposed. The methods focus on the prevention, or delayed onset or progression of, subchondral defects such as bone marrow edema or bone marrow lesion, and subchondral treatment to prevent the progression of osteoarthritis or degenerative disc disease in the spine and thereby treat pain.

CROSS-REFERENCE TO RELATED APPLICATIONS

This application is a continuation of U.S. patent application Ser. No.13/568,549 filed Aug. 7, 2012 and entitled “Subchondral Treatment ofJoint Pain of the Spine,” which application claims priority to U.S.Provisional No. 61/515,961 filed Aug. 7, 2011 and entitled “SubchondralTreatment of Joint Pain of the Spine,” the contents of which areincorporated by reference in their entirety.

FIELD

The present invention relates to methods for treating joint pain of thespine. More particularly, the present invention relates to methods toprevent the progression of degenerative disc disease or osteoarthritisof the spine by treating the subchondral bone of the vertebral body ofthe spinal segment.

BACKGROUND

Human joints are susceptible to degeneration from disease, trauma, andlong-term repetitive use that eventually lead to pain. In the spine,degenerative spine disease is a major cause of chronic disability in theadult working population. Spinal degeneration is a normal part of aging,and neck and back pain are one of life's most common infirmities.

There are many potential sources of back pain, and finding the specificcause is often a confounding problem for both patient and doctor. Paincan originate from bone, joints, ligaments, muscles, nerves andintervertebral disks, as well as other paravertebral tissues. For acutepain due to structural damage of the spine, treatments that repair thedamaged area, such as by mechanical fixation devices like fixationplates or rods, have proven effective. These treatments generallyinvolve the immobilization of the damaged area through spinerestabilization, thus altering the load sharing of each segment. This iscommonly performed by in situ, on lay, interbody, and other fusionprocedures that improve loading of the diseased subchondral defects(e.g., edema or lesions), and load transfer to other areas andimplantable devices. When fusion is not desirable, implantable motionpreservation devices may accomplish this load transfer and improvestability while reducing pain.

Unlike acute injuries or trauma of the spine, current treatments forchronic back pain due to degenerative disc disease or osteoarthritishave not proven as reliable or effective. Many medical practitionersfocus treatment on the intervertebral disc, because they have attributeddisc degeneration, more specifically the initial delamination of theannulus, followed by nucleus dehydration and subchondral bone changes,as a continuum of events as the degenerative disease cascade progresses.Current treatments comprise, for example, partial or complete fusion toimmobilize and/or isolate the damaged area, intervertebral disc repairor replacement, nucleus repair or replacement, and corpectomy.

The rationale for treating the disc as a pain source in the spine issimilar to the popular theory within the orthopedic community that jointpain, such as that found in the knee or hip, results from bone-on-bonecontact or inadequate cartilage cushioning. These conditions arebelieved to frequently result from the progression of osteoarthritis,which is measured in terms of narrowing of the joint space. Therefore,the severity of osteoarthritis is believed to be an indicator orprecursor to joint pain. Most surgeons and medical practitioners thusbase their treatments for pain relief on this theory. However, theseverity of osteoarthritis, especially in the knee, has been found tocorrelate poorly with the incidence and magnitude of knee pain. Becauseof this, surgeons and medical practitioners have struggled to deliverconsistent, reliable pain relief to patients, especially if preservationof the joint is desired. Likewise, in the spine, practitioners have notfound long-term results from chronic back pain by treating theintervertebral disc as the source and solution of mechanical loadingpain of a diseased spinal segment.

Accordingly, it would be desirable to provide a medical procedure thataddresses the pain associated with degenerative disc disease orosteoarthritis of the spine, and provides an alternative to a fusion orreplacement surgery, which can be highly invasive, risky andirreversible.

SUMMARY

The present disclosure provides methods for the treatment of pain of thespine due to osteoarthritis (OA) or degenerative disc disease (DDD). Themethods involve treating the subchondral bone to prevent themanifestation of, delay the onset or progression of, or repair anyexisting, bone marrow edema or lesion in the subchondral space.

In one embodiment, a method for treating joint pain of the spine isprovided. The method comprises: identifying a subchondral defect in asubchondral region of a bone of the spine; selecting a subchondralaccess path to a location near the subchondral defect; and treating thesubchondral defect, via the subchondral access, in a manner that reducesor relieves pain. The subchondral defect may be a bone marrow lesion orbone marrow edema, and can further include sclerotic bone or a fracture.The treatment may comprise mechanically stabilizing the defect, orstimulating a healing response to heal the defect or improve nutritionto the nucleus. The access path may be achieved through, for example,open approaches, transpedicular, and Craig needle biopsy approaches toaccess the vertebral body. The subchondral defect may be identified withMRI, x-ray, or any validated diagnostic modality that can identify bone,soft tissue, and fluid interfaces, including ultrasound and injectablelabeled and radionucleotide tagged materials that may expose and displaythese defects sufficiently to differentiate active vs. chronic defectsand healing response.

In another embodiment, a method for treating joint pain of the spine isprovided. The method comprises: identifying a subchondral defect in asubchondral region of a bone of the spine; selecting a subchondralaccess path to a location near the subchondral defect; and treating thesubchondral defect, via the subchondral access, by mechanicallystabilizing an area in or near the subchondral defect; wherein treatmentof the subchondral defect reduces or relieves pain. The treatment maycomprise implanting an implant sufficient to alter forces applied on thesubchondral defect. The treatment may also include injecting a bonehardening material such as bone cement, bone void filler, or bonesubstitute material. The access path may be achieved through, forexample, open approaches, transpedicular, and Craig needle biopsyapproaches to access the vertebral body.

In yet another embodiment, a method for treating joint pain of the spineis provided. The method comprises: identifying a subchondral defect in asubchondral region of a bone of the spine; selecting a subchondralaccess path to a location near the subchondral defect; and treating thesubchondral defect, via the subchondral access, by stimulating healingof the bone tissue in or adjacent to the subchondral defect; whereintreatment of the subchondral defect reduces or relieves pain. Healingmay be stimulated by drilling into the bone tissue via the access path,applying electrical or heat stimulation, applying biological or chemicalstimulation, or injecting a bone growth inducing material, includingallograft, autograft, bone void fillers and BMP to be used alone or withimplantable structural devices. The access path may be achieved through,for example, open approaches, transpedicular, and Craig needle biopsyapproaches to access the vertebral body.

BRIEF DESCRIPTION OF THE DRAWINGS

The accompanying drawings, which are incorporated in and constitute apart of this specification, illustrate several embodiments of thedisclosure and together with the description, serve to explain theprinciples of the disclosure.

FIG. 1 shows an exemplary functional spinal unit including its majorcomponents.

FIG. 2 illustrates the perfusion dynamics of the functional spinal unitof FIG. 1.

DESCRIPTION OF THE EMBODIMENTS

Methods for altering the natural history of degenerative disc diseaseand osteoarthritis of the spine are proposed. These methods aim toprevent, alter, therapeutically treat, and lessen structural spine painassociated with subchondral defects such as edema or lesions near andaround the cartilaginous endplate of the vertebral body and/or bothfacets of each spinal segment. It is believed that the treatment ofthese subchondral defects beneath the diseased disc segments improvesdisc loading, nutrient transfer through the subchondral plate, andrelieves pain while allowing the disc to stabilize and improve itsnatural function. Ultimately, these methods address the problem ofchronic back pain, and provide a more consistent and reliablealternative to surgical procedures like intervertebral disc replacement,nucleus replacement, annulus repair, interbody fusions, with or withoutimplanted devices, or rod-based pedicle screw system implantation.

As previously mentioned, most current treatments for back pain focus onthe disc, particularly the annulus and nucleus for the source of thefailing spinal segment with pain. Yet practitioners have not foundlong-term results from chronic back pain by treating the intervertebraldisc as the source and solution of mechanical loading pain of a diseasedspinal segment. Diagnostic tests such as MRI have helped identifydegenerative disc segments including changes in the annulus, nucleus,endplate, and subchondral bone. Other tests, such as discography, havelacked specificity and sensitivity to predictably correlate the sourceof pain with degenerative spine loading pain. Discography has been shownto advance the degeneration of the affected and tested disc when normallevels were tested. Studies showing complete fusion of degenerativesegments do not always correlate with predictable pain relief.Furthermore, subchondral defects like edema or lesions may still existon MRI even after solid fusion of motion segments. Until now, methodsfor treating pain have not focused on the supporting and nutrienttransferring subchondral bone beneath the disc space.

A technique, SUBCHONDROPLASTY™ or SCP™, for repairing damagedsubchondral bone associated with joint OA has previously been describedin U.S. application Ser. No. 12/950,355. SCP™ has proven to predictablyrelieve knee OA pain and improve patient reported quality of life. SCP™is a unique intervention allowing for the repair of damaged subchondralbone without violating the articular surface of the joint. Resolution ofBME has been shown to slow knee OA progression. That the theory behindthe identification of bone marrow edema (BME) or bone marrow lesion(BML) as the pain generator in OA and subsequent treatment of theBME/BML in subchondral bone to alleviate pain applies equally to thespine.

MRI changes of the vertebral body in DDD patients with no correlation toosteoporosis has previously been reported. Most clinicians believed thatthe annulus, and later the nucleus, were the causes of defects(edema/lesion) in the subchondral bone, and therefore treating theannulus and disc would relieve pain. In fact, these modic changes, whichare prevalent in patients with DDD, may be the root cause of pain. Anduntil now, the focus of treatments has not correlated the subchondraldefects identified as the reactive structure and source of pain.

As noted, embodiments of the present disclosure may be explained andillustrated with reference to treatment of a patient's spine. Referringnow to FIG. 1, a healthy spinal segment, or functional spinal unit, 10comprising a superior vertebral body 12 a and inferior vertebral body 12b is shown. The vertebral bodies 12 a, 12 b comprise endplates 16 whichabut an intervertebral disc 20 that resides between the vertebral bodies12 a, 12 b. As shown in FIG. 1, marrow spaces are located below thevertebral endplates 16 in the subchondral bone 14 of each of thevertebral bodies 12 a, 12 b.

In a healthy spine, the intervertebral disc 20 receives nutrients by wayof diffusion through the cartilaginous vertebral endplates 16. Thisnutrient flow dynamic, as represented by the arrows in FIG. 2, suggeststhat endplate 16 integrity plays a crucial role in the health of thedisc 20 itself. The presence of a diseased or damaged disc 20 maysuggest the lack of nutrients flowing to the disc 20 due to an unhealthyendplate 16. Moreover, these modic changes (changes to the vertebralbody) may manifest due to the presence of BME/BML in the subchondralbone of the vertebral body. Previous studies have already correlatedmodic vertebral endplate degeneration and vertebral marrow edema with adecrease in nutrient diffusion to the disc. Similar to the cartilagedamage seen in knee joints where a stressed fracture or non-union in thesubchondral bone turns into a BME over time, in the vertebral body afracture beneath the subchondral plate or non-union under stress andunable to heal itself through the body's natural reparative processthrough Wolfe's Law may manifest into BME/BML in the subchondral space.Hardened sclerotic bone may also be present, such as in the endplates16. Such hardening may represent a chronic attempt to heal thesubchondral defect, as well as a path to osteonecrosis oravascularnecrosis (AVN), as seen in the hip, knee, talus, and otherbones. This type of subchondral defect (BME/BML), along with sclerotichardening, occurs when the force on the initial fracture exceedsremodeling conditions (i.e., Wolfe's Law is rendered ineffective) and isparticularly prevalent in weight bearing joints.

In this scenario where the BME/BML becomes chronic and does not heal,pain is generated. The intervertebral disc 20 may be dying due to lackof nutrition from the sclerotic endplates 16. When the practitioner seesthe narrowing of the disc space and the general damage to the disc 20,the current tendency is to treat the disc 20 to relieve pain. However,the present disclosure proposes treating the subchondral bone to restorethe normal joint function to treat the pain with the SCP™ techniquesdisclosed, since the perceived pain is actually generated from theunderlying BME/BML in the subchondral bone and the cascade of resultingdamage that this creates, rather than the disc 20.

The SCP methods employ one or more treatment modalities to address thesubchondral bone. By subchondral bone, what is meant is any bone thatexists beneath calcifying matrix in the tidemark zone of hyalinearticular cartilage. This includes the cartilaginous endplate and thediffusion channels that originate and traverse through the subchondralspace, through the endplate, into the nucleus.

In one treatment modality, the subchondral bone can be strengthened bythe introduction of a hardening material, such as a bone substitute, inthe localized region. In another treatment modality, the subchondralbone can be stimulated to trigger or improve the body's natural healingprocess, optionally with the use of bone grafts, osteoinductive andosteoconductive materials including bone morphogenic protein (BMP). Inyet another treatment modality, an implantable device may be implantedinto the localized region of the subchondral bone to provide mechanicalsupport to the localized bone region.

The current proposed methods apply the SCP™ techniques to the spine totreat chronic pain from degenerative disc disease (DDD) orosteoarthritis (OA). The methods are intended to prevent themanifestation of any bone marrow edema or bone marrow lesion in thesubchondral bone, which as previously described is one of the underlyingroot causes for joint pain and the progression of DDD or OA in a joint.These methods involve accessing, repairing, enhancing, and/orstimulating subchondral bone in the vertebral bodies. These methodsprevent bone marrow edema or bone marrow lesions from manifesting insubchondral bone, ultimately treating the DDD and OA itself bypreventing or delaying the disease progression.

The embodiments treat the subchondral region of a spine to prevent bonemarrow edema and treat osteoarthritis or degenerative disc disease byinhibiting its progression. As previously mentioned, the methodsdisclosed are based upon the theory that back pain associated with OA orDDD can be correlated to bone defects or changes at the subchondrallevel rather than, for example, the severity of damage to the disc,including more specifically, the annulus, nucleus and the subchondralplate. In particular, bone defects, such as bone marrow lesions, edema,fissures, fractures, hardened bone, etc. near the joint surface lead toa mechanical disadvantage and abnormal stress distribution in thesubchondral bone, which may cause inflammation and generate pain. Bysubchondral bone, what is meant is any bone that exists beneathcalcifying matrix in the tidemark zone of hyaline articular cartilage.This includes the cartilaginous endplate and the diffusion channels thatoriginate and traverse through the subchondral space, through theendplate, into the nucleus. By altering the makeup of the subchondralbone (which may or may not be sclerotic) in relation to the surroundingregion, it is possible to change the structural integrity of theaffected bone and restore normal subchondral force transmission and/orstimulate bone repair, thus leading to a delay or prevention of DDD/OAsymptoms and/or DDD/OA progression.

Treatment of the bone by mechanical and/or biological means to restorethe normal physiologic stress distribution, and restore the healingbalance of the bone tissue at the subchondral level, is a more effectiveway of treating pain than conventional techniques. That is, thetreatment can be effectively achieved by: (a) mechanically strengtheningor stabilizing the subchondral bone; (b) biologically initiating orstimulating a healing response in the subchondral bone to a stresseddefect, such as, for example, an impending or actual stress fracture; or(c) both (a) and (b) combined. Accordingly, the present disclosureprovides methods for a subchondral procedure.

The subchondral techniques disclosed herein apply previously describedSCP™ methods to prevent or delay the progression of OA or DDD in thespine. These methods endeavor to treat the subchondral bone by: (a)mechanically strengthening or stabilizing the subchondral bone; (b)biologically initiating or stimulating a healing response in thesubchondral bone; or (c) both (a) and (b) combined. By doing so, SCPaims to prevent the manifestation of BME's and other subchondral defectsin the subchondral bone, which defects can lead to the progression ofthe OA/DDD and eventual increased pain and decreased joint function.Further, these methods alter the natural progressive history of OA andDDD, preventing subchondral bone forces from continually increasing byinhibiting the disease progression.

In general, these methods are similar to the SUBCHONDROPLASTY™, or SCP™,techniques and are intended to both strengthen the bone and stimulatethe bone. As with SCP, bone fractures or non-unions are stabilized,integrated or healed, which results in repair and/or resolution of abone defect, such as a bone marrow lesion or edema. In addition, themethods restore or alter the distribution of forces in the spine tothereby relieve pain. These methods can be performed arthroscopically orpercutaneously to treat a stressed fracture, preventing themanifestation of any bone marrow lesion or edema during the progressionof the OA or DDD, and avoiding or delaying the need for more risky,irreversible surgeries.

The present disclosure provides several exemplary treatment modalitiesfor the different extents of treatment needed. Accordingly, a medicalpractitioner may elect to use any of the techniques and devicesdescribed herein, either alone or in combination, to subchondrally treatthe subchondral bone as he or she deems appropriate.

The present methods provide a number of treatment modalities fortreating the subchondral bone. These treatment modalities may be usedalone or in combination. The ultimate goal of these modalities is torestore mechanical stability to the subchondral bone of the vertebralbody 12 a, 12 b of the functional spinal unit 10. In untreatedsubchondral bone, an already stressed defect, such as an impending oractual stress fracture, becomes aggravated as the disease progresses andresults in the formation of other, more severe defects like BME's. Thepresent methods aim to prevent the manifestation of BME's and othersubchondral defects in the subchondral bone, which defects can lead tothe progression of the OA/DDD and eventual increased pain and decreasedjoint function. Further, these methods alter the natural progressivehistory of OA and DDD, preventing subchondral bone forces fromcontinually increasing by inhibiting the disease progression.

In one treatment modality, the subchondral bone of the vertebral bodycan be strengthened by the introduction of a hardening material, such asa bone substitute, in the localized region. In some instances, some ofthe soft bone tissue in the localized region of the subchondral bone iscompacted prior to insertion of the hardening material. The bonesubstitute may be an injectable calcium phosphate ensconced in anoptimized carrier material. In some cases, the injected material mayalso serve as a bone stimulator that reinvigorates the bone's naturalrepair and healing activity. Treatments may include, for example,treating acid/base imbalances, treatments targeting specificneurotransmitters known to be present during painful inflammation, andthose proteins that may be specifically biopsied or assayed in thesedefects, thus leading to a specific therapy designed for that defect asa treatment, device, or injectable therapeutic.

For example, polymethylmethacrylate (PMMA) or calcium phosphate (CaP)cement injections can be made at the subchondral localized region. PMMAinjection may increase the mechanical strength of the bone, allowing itto withstand greater mechanical stresses. CaP cement injection may alsoincrease the mechanical strength of the bone, while also stimulating thelocalized region for bone fracture repair.

Suitable treatment or hardening materials include but are not limited tomaterials comprising beta-tricalcium phosphate (e.g., VITOSS, PROOSTEON500R made by E-Interpore-Cross International), hydroxyapatite (e.g.,OSTEOGRAF made by Ceramed Denta, Inc., Lakewood, Colo.), calciumcarbonate, calcium sulfate (e.g., OSTEOSET and ALLOMATRIX made by WrightMedical Technology, Inc.), calcium phosphate (e.g., CALCIBON made byMerck & Co., Inc., Whitehouse Station, N.J. and NORIAN SRS made bySynthes-Strates, Switzerland), synthetic bone fillers (e.g., CORTOSS)and/or processed bone fillers (e.g., BIOOSS made by GeistlichBiomaterials, Inc., Switzerland). Other suitable materials may includehydrogels, PEEK (polyetheretherketone), carbon fiber, polycarbonateurethane (PCU), stem cells with and without matrices, collagen with andwithout matrices and carriers, pharmacotherapeutic with and withoutmatrices and carriers, hyaluronic acid with and without matrices, insitu curable materials with and without anti-inflammatory agents,demineralized bone matrix, allograft, biocompatible metals, resorbablePCA, PGLA, and polyurethane, hydroxyapatite, calcium sulfate, BMP growthfactor, TGF-β super family, MP52, TP508, bioactive glass, sodiumalignate, AOC based carrier and active components (synthetic beeswax),and starch.

In some embodiments, the material may be of a type that can expand uponinsertion. For example, the material may be injectable at the localizedregion of the subchondral bone, whereupon it can fill up or expand intothe region. If desired, the material may also be implanted in astep-wise fashion such that an initial stage to establish primaryfixation is followed with a subsequent stage of assembly that providesadded strength and bone integration properties to the fully assembledmaterial.

In another treatment modality, the subchondral bone of the vertebralbody can be stimulated to trigger or improve the body's natural healingprocess. For example, in one embodiment of this treatment modality,small holes may be drilled at the localized region of the subchondralbone to increase stimulation (e.g., blood flow, cellular turnover, etc.)and initiate bone repair. In another embodiment, after holes are drilledan osteogenic, osteoinductive, or osteoconductive agent may beintroduced to the localized region of the subchondral bone. In addition,some of the bone tissue may be compacted in order to assist instimulating the bone tissue or create space for the introduction of bonegraft material. Bone graft material, for example, may be used to fillthe hole. This treatment modality may create a better load-supportingenvironment leading to long term healing. Electrical or heat stimulationmay also be employed to stimulate the healing process of a chronicallyinjured bone, as well as for energy induced denaturation of local nervesin and around the subchondral defects. Chemical and bio-chemicalstimulation may also be employed, including other mechanisms forgenerating a response that may favorably alter the degenerative pathwayand response to pain. Moreover, stimulation of bone tissue may beenhanced via the use of cytokines and other cell signaling agents totrigger osteogenesis, chondrogenesis, and/or angiogenesis to perhapsreverse the progression of osteoarthritis.

In yet another treatment modality, one or more implantable devices,depending on the size of the area to be treated, may be implanted intothe localized region of the subchondral bone of the vertebral body toprovide mechanical support to the localized bone region, particularlywhere an insufficiency fracture or stress fracture is present. In someembodiments, some of the bone tissue may be compacted in order to createspace for the implantable device. The implant may help create a betterload distribution in the subchondral region. In addition, the implantmay mechanically integrate with the surrounding healthy bone tissue.

The implant may further be augmented with a PMMA or CaP cementinjection, other biologic agent, or an osteoconductive, osteoinductiveand/or osteogenic agent. The augmentation material may be introducedthrough the implant, around the implant, and/or apart from the implantbut at the affected localized bone region. In addition, the implant mayalso serve as a portal to inject the augmentation material into thesubchondral bone region.

As noted, the methods described herein may provide various treatmentmodalities and employ different types of implantable devices. The mayhave various forms and shapes to maximize its surface area and reducestress of the bone when implanted. For example, the implantable devicemay be in the form of a rod having a triangular profile, a rectangularprofile, or a circular profile. The implantable device may be planar,e.g., relatively long in two dimensions and relatively short in a thirddimension. Planar implantable devices in accordance with the inventioncan have a thickness which is ≦50% of the length and ≦50% of the widthof a rectangular implantable device (or ≦50% of the diameter in the caseof a circular implantable device or ≦50% of the height and ≦50% of thebase in the case of a triangular implantable device).

In other embodiments, the implantable device may have a wedge-shapededge on at least one edge or a wedge or ramp shape when viewed from theside. A wedge-shaped edge may be adapted to facilitate inserting theimplantable device into the bone. Thus, the particular angle and otherdimensions of the wedge may be dictated by factors that are known in theart. As a wedge-shaped implant, the implantable device may be similar tostandard surgical tools, such as osteotomes, or comprise blade plates orosteotomy staples. Further, the implantable device may be an expandabledevice that can span the targeted localized region. In one embodiment,the implantable device may be an expandable screw, such as anosseoscrew.

In other embodiments, the implantable device may be in the form of aclosed disc, an open disc, a screw-shaped device, or an elongated pin.In addition, the implantable device may have a square profile,rectangular profile with rounded edges, or an I-beam profile.Alternatively, the implantable device can be an injection cementdiffuser. In some embodiments, the implantable device may beapproximately 3 mm thick.

In some embodiments, the implantable device may be customized to thepatient. For example, using 3-dimensional imaging technology, it may bedesirable to provide an implant that matches precisely the anatomicallocalized region of the subchondral bone where the implantable device isto be placed. This would ensure conformability and avoid a less thanperfect match between the implant and the targeted localized region ofthe subchondral bone.

The implantable device may be porous and/or fenestrated to allow forbone ingrowth. Implantable device comprises a physiologically compatiblematerial that has sufficient durability to reinforce the overstressedbone of the bone lesion and bear physiologic loads. Materials for theimplantable device can include metals, such as titanium, stainlesssteel, alloys of cobalt and chrome, tantalum, alloys of titanium andnickel and other superelastic metal alloys. Porous, titanium, titanium“foam”, tantalum, trabecular metals, nanoceramics, porous nitinol, orother highly porous nanomaterials, and chrome cobalt may also beemployed in the implantable device.

The implantable device may comprise a functional coating, such as,hydroxyapatite plasma coating, titanium nitrate or bioactive glass. Inaddition, the implantable device may undergo some form of surfacetreatment including acid etching, grit blast, or plasma spray. Theimplantable device may also comprise structural enhancements such asmeshes, and include autograft. The implantable device may also be formedof, or include, porous metals like tantalum or ACTIPORE.

Other embodiments comprise the use of bone, such as autografts,allografts, and artificial or synthetic bone substitutes. Certainembodiments comprise the use of polymeric materials. A combination ofmaterials, such as a porous metal applied to a carbon fiber implant maybe employed in the implantable device.

The implantable device can be osteogenic, osteoconductive, and/orosteoinductive. Osteoconductive materials that may be used include butare not limited to collagen and the various forms of calcium phosphatesincluding hydroxyapatite, tricalcium phosphate, and fluoroapatite.Suitable osteoinductive substances include but are not limited to bonemorphogenetic proteins (e.g., rhBMP-2), demineralized bone matrix,transforming growth factors (e.g., TGF-beta), osteoblast cells, andvarious other organic species known to induce bone formation. Bonemarrow, blood plasma, or morselized bone of the patient, or commerciallyavailable materials may also be used.

The implantable device may be treated prior to implantation. Forexample, the implantable device may be dipped or coated with boneconductive or bone inductive material. Osteoinductive materials, such asBMP, may be applied to, for example, by immersing the implantable devicein an aqueous solution of this material in a dilute suspension of type Icollagen. Osteoinductive materials such as TGF-beta may be applied froma saline solution containing an effective concentration of TGF-beta, ormay be carried in the resilient material. Of course, other biologics maybe applied by any method known in the art.

The implantable device can be resorbable or non-resorbable. For example,the implantable device may comprise PEEK, PGA, or PLA material.Electrical stimulation can also be applied to the bone to promote bonehealing. The implantable device may also be capable of imbibing bonestimulating material, such as porous nitinol, e.g., ACTIPORE™ or otherform of porous coated titanium or periapatite coated titanium.

In some embodiments, implantation of the implantable device may beachieved step-wise in multiple stages. For example, the implantabledevice may be constructed to be implanted at an initial stage toestablish primary fixation, then at a subsequent stage additionalimplantation or assembly can be performed to add increased pull-outstrength and other reinforcing properties to the fully assembledimplantable device.

Other forms of implantable devices and variations of the implantabledevice are also disclosed in co-pending and co-owned U.S. patentapplication Ser. No. 12/950,306, filed Nov. 19, 2010 and entitled“IMPLANTABLE DEVICES FOR SUBCHONDRAL TREATMENT OF JOINT PAIN,” U.S.patent application Ser. No. 12/950,273, filed Nov. 19, 2010 and entitled“IMPLANTABLE DEVICES FOR SUBCHONDRAL TREATMENT OF JOINT PAIN,” and U.S.patent application Ser. No. 12/950,183, filed Nov. 19, 2010 and entitle“BONE-DERIVED IMPLANTABLE DEVICES FOR SUBCHONDRAL TREATMENT OF JOINTPAIN,” the contents of which are herein incorporated in their entiretyby reference.

While each of the above-mentioned treatment modalities may beadministered independent of one another, it is contemplated that anycombination of these modalities may be applied together and in any orderso desired, depending on the severity of the OA or DDD.

Other embodiments of the invention will be apparent to those skilled inthe art from consideration of the specification and practice of thedisclosure provided herein. It is intended that the specification andexamples be considered as exemplary only, with a true scope and spiritof the disclosure being indicated by the following claims.

1. (canceled)
 2. A method of reinforcing bone located in a targeted bonemarrow lesion (BML) in a subchondral region of a vertebral body of apatient for treating the targeted bone marrow lesion, the methodcomprising: identifying a bone marrow lesion in a subchondral region ofa vertebral body of a patient so as to establish a targeted bone marrowlesion for receiving treatment, the vertebral body including a superiorcartilaginous endplate abutting a first intervertebral disc and aninferior cartilaginous endplate abutting a second intervertebral disc;creating, in the vertebral body that contains the targeted bone marrowlesion in the subchondral region, a subchondral injection path to anarea in and/or adjacent to the targeted bone marrow lesion for injectingan injectable bone filling material into said area for reinforcing bonelocated in the targeted bone marrow lesion; and injecting an injectableand curable bone filling material into said area via the subchondralinjection path, wherein the injectable bone filling material is a bonereinforcing material that is left in the area for hardening in the areaso as to form, in situ, a bone reinforcing member for reinforcing bonelocated in the targeted bone marrow lesion.
 3. The method of claim 2,wherein said identifying includes identifying with MRI.
 4. The method ofclaim 2, wherein the injectable bone filling material is left in thearea without also delivering and leaving a structural implant device inand/or adjacent to the targeted bone marrow lesion in addition to theinjectable bone filling material.
 5. The method of claim 2, wherein saidcreating is conducted without further creating a void in or adjacent tothe targeted bone marrow lesion.
 6. The method of claim 2, wherein theinjectable bone filling material envelopes the targeted bone marrowlesion.
 7. The method of claim 2, wherein said creating is performedpercutaneously.
 8. The method of claim 2, wherein said creating isperformed arthroscopically.
 9. The method of claim 2, wherein saidcreating preserves an existing condition of the superior cartilaginousendplate of the vertebral body and an existing condition of the inferiorcartilaginous endplate of the vertebral body.
 10. The method of claim 2,wherein the subchondral injection path is created with a needle.
 11. Themethod of claim 2, wherein said area is in the targeted bone marrowlesion.
 12. A method of reinforcing bone located in a targeted bonemarrow lesion (BML) in a subchondral region of a vertebral body of apatient for treating the targeted bone marrow lesion, the methodcomprising: identifying a bone marrow lesion in a subchondral region ofa vertebral body of a patient so as to establish a targeted bone marrowlesion for receiving treatment, the vertebral body including a superiorcartilaginous endplate abutting a first intervertebral disc and aninferior cartilaginous endplate abutting a second intervertebral disc;creating, in the vertebral body that contains the targeted bone marrowlesion in the subchondral region, a subchondral injection path to anarea in and/or adjacent to the targeted bone marrow lesion for injectingan injectable bone filling material into said area for reinforcing bonelocated in the targeted bone marrow lesion; and injecting an injectableand curable bone filling material into the targeted bone marrow lesionvia the subchondral injection path, wherein the injectable bone fillingmaterial is a bone reinforcing material that is left in the targetedbone marrow lesion for hardening in the targeted bone marrow lesion soas to form, in situ, a bone reinforcing member for reinforcing bonelocated in the targeted bone marrow lesion.
 13. The method of claim 12,wherein said identifying includes identifying with MRI.
 14. The methodof claim 12, wherein the injectable bone filling material is left in thearea without also delivering and leaving a structural implant device inand/or adjacent to the targeted bone marrow lesion in addition to theinjectable bone filling material.
 15. The method of claim 12, whereinsaid creating is conducted without further creating a void in oradjacent to the targeted bone marrow lesion.
 16. The method of claim 12,wherein said creating is performed percutaneously.
 17. The method ofclaim 12, wherein said creating is performed arthroscopically.
 18. Themethod of claim 12, wherein the subchondral injection path is createdwith a needle.
 19. The method of claim 12, wherein said area is in thetargeted bone marrow lesion.
 20. A method of reinforcing bone located ina targeted bone marrow lesion (BML) in a subchondral region of avertebral body of a patient for treating the targeted bone marrowlesion, the method comprising: identifying a bone marrow lesion in asubchondral region of a vertebral body of a patient so as to establish atargeted bone marrow lesion for receiving treatment, the vertebral bodyincluding a superior cartilaginous endplate abutting a firstintervertebral disc and an inferior cartilaginous endplate abutting asecond intervertebral disc; creating, in the vertebral body thatcontains the targeted bone marrow lesion in the subchondral region, asubchondral injection path to an area in and/or adjacent to the targetedbone marrow lesion for injecting an injectable bone filling materialinto said area for reinforcing bone located in the targeted bone marrowlesion; and injecting an injectable and curable bone filling materialinto the targeted bone marrow lesion via the subchondral injection path,wherein the injectable bone filling material is a bone reinforcingmaterial that is left in the targeted bone marrow lesion for hardeningin the targeted bone marrow lesion so as to form, in situ, a bonereinforcing member for reinforcing bone located in the targeted bonemarrow lesion, and wherein the injectable bone filling materialenvelopes the targeted bone marrow lesion.
 21. The method of claim 20,wherein the injectable bone filling material is left in the targetedbone marrow lesion without also delivering and leaving a structuralimplant device in and/or adjacent to the targeted bone marrow lesion inaddition to the injectable bone filling material.
 22. The method ofclaim 20, wherein said creating is conducted without further creating avoid in or adjacent to the targeted bone marrow lesion.